Data have suggested a role for chronic Chlamydia pneumoniae infection in human atherosclerosis, however a direct causal role remains to be established. Elucidation of potential pathogenic mechanisms is critical to establishing whether C. pneumoniae actually possesses biological features consistent with a significant role in the initiation or exacerbation of this disease. Proteome analysis can be useful in elucidation of potential functions of expressed proteins, since changes in the bacterial proteome depend on growth stages, disease states or environmental conditions. Analysis of gene expression can also be determined via quantification of specific mRNA of a predetermined set of genes. A combination of transcriptomics and proteomics would provide a total picture of C. pneumoniae gene expression at any given time point. Evidence exists which localizes C. pneumoniae within cells of human atheromas. Thus, in order for C. pneumoniae to plan a causative role in atherogenesis, it would need to persist within intimal tissue for extended periods of time, thereby stimulating a chronic inflammatory response. An alteration of the normal growth cycle can be induced, in vitro, leading to the induction of a persistent form of the organism. More importantly, an alteration in gene expression patters, as well as the resulting Proteome, has been identified in the persistent forms of the bacterium. It is proposed that persistence of C. pneumoniae in cells of the developing atheroma, a microenvironment containing a multitude of host pro-inflammatory cytokines, could induce differential expression of specific bacterial proteins. Such proteins could serve as virulence factors or immunogens of C. pneumoniae. Modulated proteins of persistent C. pneumoniae in cell culture will be identified by mRNA and proteomics analysis, sequenced, expressed in an appropriate vector and specific antibodies. Such reagents could be used to probe infected cell cultures as confirmation step prior to their future use in probing human tissue specimens suspected of harboring persistent C.pneumoniae.